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Am J Physiol Cell Physiol 283: C282-C288, 2002. First published March 20, 2002; doi:10.1152/ajpcell.00437.2001
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Vol. 283, Issue 1, C282-C288, July 2002

Phosphatidylinositol 3-kinase-dependent, MEK- independent proliferation in response to CaR activation

Tim R. Bilderback1, Fred Lee1, Nelly Auersperg2, and Karin D. Rodland1,3

1 Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon 97201-3098; 2 University of British Columbia, Vancouver, British Columbia, Canada V6H 3V5; and 3 Pacific Northwest National Laboratory, Richland, Washington 99352

Although ovarian surface epithelial (OSE) cells are responsible for the majority of ovarian tumors, we know relatively little about the pathway(s) that is responsible for regulating their proliferation. We found that phosphatidylinositol 3-kinase (PI3K) is activated in OSE cells in response to elevated extracellular calcium, and the PI3K inhibitors wortmannin and LY-294002 inhibited extracellular signal-regulated kinase (ERK) activation by ~75%, similar to effects of the mitogen-activated protein kinase/ERK kinase inhibitor PD-98059. However, in assays of proliferation, we found that PD-98059 inhibited proliferation by ~50%, whereas wortmannin inhibited >90% of the proliferative response to elevated calcium. Expression of a dominant negative PI3K totally inhibited ERK activation in response to calcium. These results demonstrate that ERK activation cannot account for the full proliferative effect of elevated calcium in OSE cells and suggest the presence of an ERK-independent, PI3K-dependent component in the proliferative response.

ovarian surface epithelial cells; signal transduction; extracellular signal-regulated kinase; mitogen-activated protein kinase; Akt; calcium-sensing receptor


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